Modulation of mitochondrial function and autophagy mediates carnosine neuroprotection against ischemic brain damage.

ABSTRACT:

Background and purpose

Despite the rapidly increasing global burden of ischemic stroke, no therapeutic options for neuroprotection against stroke currently exist. Recent studies have shown that autophagy plays a key role in ischemic neuronal death, and treatments that target autophagy may represent a novel strategy in neuroprotection. We investigated whether autophagy is regulated by carnosine, an endogenous pleiotropic dipeptide that has robust neuroprotective activity against ischemic brain damage.

Methods

We examined the effect of carnosine on mitochondrial dysfunction and autophagic processes in rat focal ischemia and in neuronal cultures.

Results

Autophagic pathways such as reduction of phosphorylated mammalian target of rapamycin (mTOR)/p70S6K and the conversion

SUBMITTER: Baek SH 

PROVIDER: S-EPMC4211270 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature